Estimation of Breath Holding Time (BHT) among Dental Students

Background: Breath holding time is the time taken by an individual to hold his/her breath as long as they can. During voluntary breath holding, tissues continue to utilize oxygen and liberate carbon dioxide. Therefore, during breath holding arterial pO2 falls and pCO2 rises. Normal Breath holding time (BHT) is 45-55 seconds which is estimated at 2014. The main aim of this study is to assess the breath holding time among healthy dental students. Materials and Methods: A minimal number of sample sizes have been taken into account with regards to their BMI. The sample size was divided into two groups as gender comparison. Students were detail explained about the procedure and breath holding time has been measured. The statistical analysis was done by ANOVA test in SPSS Software-23 and an independent t-test was calculated. Results: BHT was found to be significantly low among females compared to males. A statistically significant negative correlation was observed when BHT is correlated with gender because BHT differs in both the gender. Conclusion: The present study revealed that breath holding time is less in females compared to males. Therefore, males are healthier than females.

Target arterial PO2 according to the underlying pathology: a mini-review of the available data in mechanically ventilated patients

There is an ongoing discussion whether hyperoxia, i.e. ventilation with high inspiratory O2 concentrations (FIO2), and the consecutive hyperoxaemia, i.e. supraphysiological arterial O2 tensions (PaO2), have a place during the acute management of circulatory shock. This concept is based on experimental evidence that hyperoxaemia may contribute to the compensation of the imbalance between O2 supply and requirements. However, despite still being common practice, its use is limited due to possible oxygen toxicity resulting from the increased formation of reactive oxygen species (ROS) limits, especially under conditions of ischaemia/reperfusion. Several studies have reported that there is a U-shaped relation between PaO2 and mortality/morbidity in ICU patients. Interestingly, these mostly retrospective studies found that the lowest mortality coincided with PaO2 ~ 150 mmHg during the first 24 h of ICU stay, i.e. supraphysiological PaO2 levels. Most of the recent large-scale retrospective analyses studied general ICU populations, but there are major differences according to the underlying pathology studied as well as whether medical or surgical patients are concerned. Therefore, as far as possible from the data reported, we focus on the need of mechanical ventilation as well as the distinction between the absence or presence of circulatory shock. There seems to be no ideal target PaO2 except for avoiding prolonged exposure (> 24 h) to either hypoxaemia (PaO2 < 55–60 mmHg) or supraphysiological (PaO2 > 100 mmHg). Moreover, the need for mechanical ventilation, absence or presence of circulatory shock and/or the aetiology of tissue dysoxia, i.e. whether it is mainly due to impaired macro- and/or microcirculatory O2 transport and/or disturbed cellular O2 utilization, may determine whether any degree of hyperoxaemia causes deleterious side effects.

How Do We Monitor Oxygenation During The Management of PPHN? Alveolar, Arterial or Mixed Oxygen Tension or Peripheral Saturation?

Oxygen is a pulmonary vasodilator and plays an important role in mediating circulatory transition from fetal and postnatal period. Alveolar oxygen tension (PAO2) and pulmonary arterial PO2 are the main factors that influence hypoxic pulmonary vasoconstriction (HPV). Inability to achieve adequate pulmonary vasodilation at birth leads to persistent pulmonary hypertension of the newborn (PPHN). Supplemental oxygen is the mainstay of PPHN management. However, optimal monitoring of oxygenation to achieve low pulmonary vascular resistance (PVR) and optimize oxygen delivery to vital organs is not known. Noninvasive pulse oximetry measures peripheral saturations (SpO2) and ranges 91-95% are recommended during acute PPHN management. However, for a given SpO2, there is wide variability in arterial oxygen tension, especially with variations in hemoglobin type (transfusions), pH and body temperature. This review evaluates the role of alveolar, preductal, postductal, and mixed venous oxygen tension and SpO2 in the management of PPHN. Translation and clinical studies suggest maintaining an arterial oxygen tension of 50-80 mmHg to help decrease PVR and optimize pulmonary vasodilator management. Nevertheless, there are no randomized clinical trials evaluating outcomes in PPHN based on targeting SpO2 or PO2. However, most critically ill patients have umbilical arterial catheters and postductal arterial oxygenation may not be an accurate assessment of oxygen delivery to vital organs or factors influencing HPV. The mixed venous oxygen tension from umbilical venous catheter blood gas may assess pulmonary arterial PO2 and potentially predict HPV. It is crucial to conduct randomized controlled studies with different PO2/SpO2 ranges and compare outcomes in PPHN.

Obesity decreases the contribution of Kv channels to hypoxic coronary vasodilation

Background and Hypothesis: Our group previously demonstrated that reductions in the functional expression of voltage-dependent K+ (Kv) channels contribute to impaired metabolic control of coronary blood flow in the setting of obesity. This study tested the hypothesis that obesity diminishes the contribution of Kv channels to coronary vasodilation in response to hypoxemia. Experimental Design or Project Methods: Control lean (n = 7) and obese (n = 5) swine were anesthetized and the heart exposed via left lateral thoracotomy. Coronary blood flow was measured in response to hypoxemia, before and after inhibition of Kv channels by 4-aminopyridine (4-AP; 0.3 mg/kg, iv), by a flow probe placed about the left anterior descending coronary artery. Hypoxemia was induced by progressive increases in the amount of nitrogen introduced into the ventilator. Arterial blood samples were obtained at each reduction in arterial oxygenation via a catheter placed in the femoral artery. Results: Blood pressure decreased from ~88 ± 5 mmHg to ~68 ± 6 mmHg (P = 0.01) as arterial PO2 was reduced below 50 mmHg in both lean and obese swine (P = 0.51). In lean swine, coronary flow progressively increased from ~0.6 to >3.0 ml/min/g as arterial PO2 was reduced. This response was decreased by ~40% in obese swine and by ~30% in lean swine treated with 4-AP. Administration of 4AP had no effect on coronary flow in obese swine. Conclusion and Potential Impact: These data support that Kv channels contribute to increases in coronary flow in response to hypoxemia in lean swine and that reductions in Kv channel function contribute to impaired hypoxic coronary vasodilation in obese swine. We propose that therapeutic targeting of obesity associated pathways (angiotensin-aldosterone system) known to influence K+ channel expression could improve coronary microvascular function and cardiovascular outcomes in subjects with obesity. Supported by R01 HL136386; T35 HL 110854.

Gas exchange assessment in the critically ill

Chapter 75 laid out the basic principles that govern pulmonary gas exchange, a step necessary for the appropriate application and interpretation of common clinical tests of gas exchange. The present chapter discusses the several common tests and indices used to analyse and quantify gas exchange abnormalities in critically-ill patients. There is special emphasis on inherent limitations of each technique, as well as on ways to minimize technical and experimental errors when the necessary measurements are made. Limitations and errors are considered to be of major clinical importance because, while the measurements and indices themselves are easy to obtain, and have been in routine use for many years, serious errors of interpretation can occur if the limitations and common errors are not appreciated and allowed for. In particular, it is pointed out that factors external to the lungs can dramatically change arterial oxygenation in the critically-ill patient. This means that not all changes in gas exchange reflect changes in lung pathology. It is not uncommon for arterial PO2 to change without change in lung disease severity when external factors such as metabolic rate, cardiac output, and blood temperature change.